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Fixed Volume or Fixed Pressure: A Murine Model of Hemorrhagic Shock
Published on: June 6, 2011
Intestinal microcirculation and mucosal oxygenation during hemorrhagic shock and resuscitation at different inspired
Nicolas Libert1, Anatole Harrois, Nathalie Baudry
1From the Laboratoire d'Etude de la Microcirculation (N.L., N.B.), Université Paris 7, Hôpitaux Saint Louis Lariboisière, Assistance Publique-Hôpitaux de Paris, Paris; Service d'Anesthésie-Réanimation (N.L.), Hopital d'Instruction des Armées Percy, Clamart; Service d'Anesthésie-Réanimation Chirurgicale (A.H., J.D.), Hôpital de Bicêtre, Université Paris-Sud, Hôpitaux Universitaires Paris-Sud, Assistance Publique-Hôpitaux de Paris, Le Kremlin Bicêtre; and Unité de Recherche Clinique (E.V.), Université Paris 7, Hôpitaux Saint Louis Lariboisière, Assistance Publique-Hôpitaux de Paris, Paris, France.
Background:
Hypotensive resuscitation is the standard of care of hemorrhagic shock resuscitation. The optimal level of arterial pressure is debated and there is a lack of data on relationships between arterial pressure, microcirculation and tissue oxygenation. We investigated the relationship between mean arterial pressure, intestinal microcirculation and mucosal oxygen tension during hemorrhagic shock and resuscitation at different inspired oxygen fraction concentration.
Methods:
The study was divided into two phases: 32 mice were progressively exsanguinated and then transfused in mean arterial pressure (MAP)-titrated steps of 10 mm Hg. Mice were randomized to four experimental groups: a control group in which sham mice underwent a laparotomy and three interventional groups with a common phase of exsanguination followed by progressive resuscitation at three different inspired oxygen concentrations (FIO2) (15%, 30%, and 100%). Intestinal mucosal oxygenation (intestinal PO2) and microcirculatory parameters were recorded at each 10 mm Hg MAP step.
Results:
During exsanguination, intestinal PO2 decreased linearly with MAP levels. Microcirculatory parameters decreased nonlinearly with MAP levels while they had a linear relationship with intestinal PO2. Intestinal mucosal hypoxia (PO2 ≤ 20 mm Hg) began at a MAP of 60 mm Hg and MAP < 60 mm Hg was associated with a high percentage of animal with intestinal hypoxia (≥32%). Combination of MAP and microcirculatory parameters was superior to MAP alone at predicting mucosal oxygenation. Inversely, during resuscitation with FIO2 = 30%, the microcirculatory parameters increased linearly with MAP levels while they had a nonlinear relationship with intestinal PO2. Hypoxia (FIO2 = 15%) was poorly tolerated. In hyperoxic group (FIO2 = 100%) intestinal PO2 became significantly higher than baseline values as soon as 50 mm Hg MAP.
Conclusion:
During hemorrhagic shock, intestinal PO2 decreased linearly with MAP levels and microcirculatory parameters. Associating MAP and microcirculatory parameters allowed a better prediction of intestinal PO2 than MAP alone. A MAP < 60 mm Hg was associated with a high percentage of animal with intestinal hypoxia. Normoxic resuscitation (FIO2 = 30%) was sufficient to restore intestinal PO2.
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